Chapter 38: Vascular Disorders
PERIPHERAL ARTERIAL DISEASE
Peripheral arterial disease (PAD) is a progressive narrowing and degeneration of the
arteries of the neck, abdomen, and extremities. In most cases, it is a result of
PAD typically appears in the sixth to eighth decades of life. It occurs at an earlier age in
persons with diabetes mellitus and more frequently in African Americans.
The four most significant risk factors for PAD are cigarette smoking (most important),
hyperlipidemia, hypertension, and diabetes mellitus.
The most common locations for PAD are the coronary arteries, carotid arteries, aortic
bifurcation, iliac and common femoral arteries, profunda femoris artery, superficial
femoral artery, and distal popliteal artery.
Aortic aneurysms are outpouchings or dilations of the arterial wall.
The primary causes of aortic aneurysms can be classified as degenerative, congenital,
mechanical, inflammatory, or infectious.
Aortic aneurysms may involve the aortic arch, thoracic aorta, and/or abdominal aorta, but
most are found in the abdominal aorta below the level of the renal arteries.
Thoracic aorta aneurysms are often asymptomatic, but the most common manifestations
are deep, diffuse chest pain that may extend to the interscapular area; hoarseness as a
result of pressure on the recurrent laryngeal nerve; and dysphagia from pressure on the
Abdominal aortic aneurysms (AAAs) are often asymptomatic but symptoms may mimic
pain associated with abdominal or back disorders.
The most serious complication related to an untreated aneurysm is rupture and bleeding.
Diagnostic tests for AAAs include chest x-ray, electrocardiogram (to rule out myocardial
infarction), echocardiography, CT scan, and magnetic resonance imaging scan.
The goal of management is to prevent the aneurysm from rupturing.
Surgical repair of AAA involves (1) incising the diseased segment of the aorta, (2)
removing intraluminal thrombus or plaque, (3) inserting a synthetic graft, and (4) suturing
the native aortic wall around the graft. Minimally invasive endovascular grafting is an alternative to conventional surgical repair
of AAA and involves the placement of a sutureless aortic graft into the abdominal aorta
inside the aneurysm via a femoral artery cutdown.
Preoperatively, the patient is monitored for indications of aneurysm rupture.
Preoperative teaching should include a brief explanation of the disease process, the
planned surgical procedure(s), preoperative routines, and what to expect immediately
The overall goals for a patient undergoing aortic surgery include (1) normal tissue
perfusion, (2) intact motor and sensory function, and (3) no complications related to
surgical repair, such as thrombosis or infection.
Postoperatively, the patient will have an endotracheal tube for mechanical ventilation, an
arterial line, a central venous pressure or pulmonary artery catheter, peripheral
intravenous lines, an indwelling urinary catheter, a nasogastric tube, and continuous ECG
and pulse oximetry monitoring.
o Monitoring for graft patency and adequate renal perfusion are priorities;
maintenance of an adequate BP is extremely important.
o Antibiotics are given to prevent infection.
o Peripheral pulses, skin temperature and color, capillary refill time, and sensation
and movement of the extremities are assessed and recorded per hospital policy.
o Hourly urine outputs and daily weights are recorded.
On discharge, the patient should be instructed to gradually increase activities but to avoid
heavy lifting for at least 4 to 6 weeks.
Expected outcomes for the patient who undergoes aortic surgery include (1) patent
arterial graft with adequate distal perfusion, (2) adequate urine output, (3) normal body
temperature, and (4) no signs of infection.
Aortic dissection occurs most commonly in the thoracic aorta and is the result of a tear
in the intimal (innermost) lining of the arterial wall allowing blood to “track” between the
intima and media and creates a false lumen of blood flow.
The exact cause of aortic dissection is uncertain, and most people with dissection are
older and have chronic hypertension.
Clinical manifestations include a sudden, severe pain in the anterior part of the chest or
intrascapular pain radiating down the spine into the abdomen or legs that is described as
“tearing” or “ripping.”
Diagnostic studies used to assess aortic dissection are similar to those performed for
AAA. The initial goal of therapy for aortic dissection without complications is to lower the BP
and myocardial contractility with drug therapy.
Surgery is indicated when drug therapy is ineffective or when complications of aortic
dissection are present.
PERIPHERAL ARTERIAL DISEASE OF THE LOWER EXTREMITIES
PAD of the lower extremities affects the aortoiliac, femoral, popliteal, tibial, or peroneal
The classic symptom of PAD of the lower extremities is intermittent claudication,
which is defined as ischemic muscle ache or pain that is precipitated by a consistent level
of exercise, resolves within 10 minutes or less with rest, and is reproducible.
Paresthesia, manifested as numbness or tingling in the toes or feet, may result from nerve
tissue ischemia. Gradually diminishing perfusion to neurons produces loss of both
pressure and deep pain sensations.
Physical findings include thin, shiny, and taut skin; loss of hair on the lower legs;
diminished or absent pedal, popliteal, or femoral pulses; pallor or blanching of the foot in
response to leg elevation (elevation pallor); and reactive hyperemia (redness of the foot)
when the limb is in a dependent position (dependent rubor).
Rest pain most often occurs in the forefoot or toes, is aggravated by limb elevation, and
occurs when there is insufficient blood flow to maintain basic metabolic requirements of
the tissues and nerves of the distal extremity.
Complications of PAD include nonhealing ulcers over bony prominences on the toes,
feet, and lower leg, and gangrene. Amputation may be required if blood flow is not
Tests used to diagnose PAD include Doppler ultrasound with segmental blood pressures
at the thigh, below the knee, and at ankle level. A falloff in segmental BP of more than 30
mm Hg indicates PAD.
Angiography is used to delineate the location and extent of the disease process.
The first treatment goal is to aggressively modify all cardiovascular risk factors in all
patients with PAD, with smoking cessation a priority.
Drug therapy includes antiplatelet agents and ACE inhibitors. Two drugs are approved to
treat intermittent claudication, pentoxifylline (Trental) and cilostazol (Pletal).
The primary nonpharmacologic treatment for claudication is a formal exercise-training
program with walking being the most effective exercise. Ginkgo biloba has been found to increase walking distance for patients with intermittent
Critical limb ischemia is a chronic condition characterized by ischemic rest pain, arterial
leg ulcers, and/or gangrene of the leg due to advanced PAD.
Interventional radiologic procedures for PAD include percutaneous transluminal balloon
angioplasty. There is a relatively high rate of restenosis after balloon angioplasty.
The most common surgical procedure for PAD is a peripheral arterial bypass operation
with autogenous vein or synthetic graft material to bypass or carry blood around the
The overall goals for the patient with lower extremity PAD include (1) adequate tissue
perfusion, (2) relief of pain, (3) increased exercise tolerance, and (4) intact, healthy skin
After surgical or radiologic intervention, the operative extremity should be checked every
15 minutes initially and then hourly for skin color and temperature, capillary refill,
presence of peripheral pulses, and sensation and movement of the extremity.
All patients with PAD should be taught the importance of meticulous foot care to prevent
Acute arterial ischemia is a sudden interruption in the arterial blood supply to tissue, an
organ, or an extremity that, if left untreated, can result in tissue death.
Signs and symptoms of an acute arterial ischemia usually have an abrupt onset and
include the “six Ps:” pain, pallor, pulselessness, paresthesia, paralysis, and poikilothermia
(adaptation of the ischemic limb to its environmental temperature, most often cool).
Treatment options include anticoagulation, thrombolysis, embolectomy, surgical
revascularization, or amputation.
THROMBOANGIITIS OBLITERANS (BUERGER’S DISEASE)
Thromboangiitis obliterans is a somewhat rare nonatherosclerotic, segmental, recurrent
inflammatory vaso-occlusive disorder of the small and medium-sized arteries, veins, and
nerves of the upper and lower extremities.
Patients may have intermittent claudication of the feet, hands, or arms.
As the disease progresses, rest pain and ischemic ulcerations develop.
There are no laboratory or diagnostic tests specific to Buerger’s disease. Treatment includes complete cessation of tobacco use in any form (including secondhand
smoke). Other therapies can be considered but have had limited success.
Surgical options include revascularization and sympathectomy, with the most common
being sympathectomy (transection of a nerve, ganglion, and/or plexus of the sympathetic
Raynaud’s phenomenon is an episodic vasospastic disorder of small cutaneous arteries,
most frequently involving the fingers and toes. The exact etiology of Raynaud’s
phenomenon remains unknown.
Clinical symptoms include vasospasm-induced color changes of the fingers, toes, ears,
and nose (white, blue, and red). An episode usually lasts only minutes but in severe cases
may persist for several hours.
Symptoms usually are precipitated by exposure to cold, emotional upsets, caffeine, and
There is no simple diagnostic test for Raynaud’s phenomenon, and diagnosis is based on
persistent symptoms for at least 2 years.
Patient teaching should be directed toward prevention of recurrent episodes: temperature
extremes and all tobacco products should be avoided.
Calcium channel blockers are the first-line drug therapy.
Venous thrombosis is the most common disorder of the veins and involves the formation
of a thrombus (clot) in association with inflammation of the vein.
Superficial thrombophlebitis occurs in about 65% of all patients receiving IV therapy
and is of minor significance.
Deep vein thrombosis (DVT) involves a thrombus in a deep vein, most commonly the
iliac and femoral veins, and can result in embolization of thrombi to the lungs.
Three important factors (called Virchow’s triad) in the etiology of venous thrombosis
are (1) venous stasis, (2) damage of the endothelium, and (3) hypercoagulability of the
Superficial thrombophlebitis presents as a palpable, firm, subcutaneous cordlike vein.
The area surrounding the vein may be tender to the touch, reddened, and warm. A mild
systemic temperature elevation and leukocytosis may be present.
o Treatment of superficial thrombophlebitis includes elevating the affected
extremity to promote venous return and decrease the edema and applying warm, moist heat.
o Mild oral analgesics such as acetaminophen or aspirin are used to relieve pain.
The patient with DVT may or may not have unilateral leg edema, extremity pain, warm
skin, erythema, and a sy